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本文引用的文献
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Preexposure of mouse peritoneal macrophages to lipopolysaccharide and other stimuli enhances the nitric oxide response to secondary stimuli.
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Lipopolysaccharide-induced selective priming effects on tumor necrosis factor alpha and nitric oxide production in mouse peritoneal macrophages.
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Selective refractoriness of macrophages to endotoxin-induced production of tumor necrosis factor, elicited by an autocrine mechanism.
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Necessity and sufficiency of beta interferon for nitric oxide production in mouse peritoneal macrophages.
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Regulation of tumour necrosis factor-alpha processing by a metalloproteinase inhibitor.
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Processing of tumour necrosis factor-alpha precursor by metalloproteinases.
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Increased nitric oxide synthesis during the development of endotoxin tolerance.
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Pre-exposure of murine macrophages to lipopolysaccharide inhibits the induction of nitric oxide synthase and reduces leishmanicidal activity.
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Endotoxin-induced expression of endotoxin binding sites on murine bone marrow cells.
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Tumor necrosis factor alpha acts as an autocrine second signal with gamma interferon to induce nitric oxide in group B streptococcus-treated macrophages.
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